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Comparative study of the effect of luminal hypotonicity on mucosal permeability in rat upper gastrointestinal tract
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology. (Nylander)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology. (Nylander)
2008 (English)In: Acta Physiologica, ISSN 1748-1708, Vol. 193, no 1, 67-78 p.Article in journal (Refereed) Published
Abstract [en]

Aim: To investigate whether the increase in mucosal permeability in the duodenum, induced by luminal hypotonicity, also occurs in the stomach and the jejunum and whether this increase in permeability can be explained by epithelial injury. Methods: The stomach, duodenum or jejunum of the anaesthetized rat were perfused with a hypotonic solution and effects on mucosal permeability (blood-to-lumen clearance of radioactive probes); luminal alkalinization and net fluid flux were determined in the absence and presence of cyclooxygenase inhibition. Results: The hypotonicity-induced (50 mM NaCl) increase in duodenal mucosal permeability was markedly larger in cyclooxygenase-2-inhibited animals than in controls and associated with a 20% decrease in luminal alkalinization and increased fluid absorption. Perfusion with 50 mM NaCl increased duodenal mucosal permeability to all probes investigated, i.e. C-14-urea, C-14-methyl-D-glucose, Cr-51-EDTA and C-14-inulin. The percentage increase in permeability was the greatest for inulin and the lowest for urea. Luminal hypotonicity caused superficial villous tip damage in some but not in all duodenal specimens but there was no difference in morphology between controls and cyclooxygenase-2-inhibited animals. Jejunum, but not the stomach, responded to luminal hypotonicity by increasing net fluid absorption, mucosal permeability (greater than sixfold) and the rate of luminal alkalinization (> 100%). Conclusions: The stomach does not respond while the jejunum is more sensitive to hypotonicity-induced increase in mucosal permeability than the duodenum. The hypotonicity-induced increase in duodenal mucosal permeability most probably constitutes a physiological mechanism that entails widening of paracellular pathways, which facilitates the transport of osmolytes into the lumen.

Place, publisher, year, edition, pages
2008. Vol. 193, no 1, 67-78 p.
National Category
Physiology Gastroenterology and Hepatology
Identifiers
URN: urn:nbn:se:uu:diva-95370DOI: 10.1111/j.1748-1716.2007.01777.xISI: 000254639300007PubMedID: 18005215OAI: oai:DiVA.org:uu-95370DiVA: diva2:169553
Available from: 2007-01-12 Created: 2007-01-12 Last updated: 2009-11-12Bibliographically approved
In thesis
1. Luminal Hypotonicity and Duodenal Functions: An Experimental Study in the Rat
Open this publication in new window or tab >>Luminal Hypotonicity and Duodenal Functions: An Experimental Study in the Rat
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

After drinking water, the fluid quickly leaves the stomach thereby creating a hypotonic luminal environment in the duodenum. This in turn constitutes a potential threat to the integrity of the duodenal epithelium. It therefore seems highly likely that luminal hypotonicity activates physiological mechanisms that aim to increase luminal osmolality. One such physiological mechanism may be to increase mucosal permeability thereby facilitating the transport of osmolytes into the lumen.

A draw-back of performing experiments in anesthetized animals is that surgery per se depresses gut functions, such as peristalsis, by mechanisms involving endogenous prostaglandins. In this thesis it is shown that inhibition of cyclooxygenase-2 (COX-2), in animals subjected to an abdominal operation, restore and/or improve duodenal functions such as motility, mucosal bicarbonate secretion, hypotonicity-induced increase in mucosal permeability and the osmolality-adjusting capability.

Experiments revealed that the stomach is resistant to hypotonic challenge while the jejunum is more sensitive to hypotonicity-induced increase in mucosal permeability than the duodenum. The hypotonicity-induced increase in duodenal mucosal permeability is not due to injury but possibly reflects physiological dilatation of paracellular shunts.

Luminal perfusion of the duodenum with an isotonic solution lacking Cl- decreased bicarbonate secretion while the lack of luminal Na+ increased mucosal permeability. Stimulation of bicarbonate secretion by COX-2 inhibition is to a large extent dependent on luminal Cl- while that induced by vasoactive intestinal peptide is not.

The hypotonicity-induced increase in mucosal permeability involves the release and action of serotonin (5-HT) on 5-HT3 and 5-HT4 receptors and stimulation of enteric nerves strongly implicating physiological regulation of this process.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 59 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 217
Keyword
Physiology, luminal alkalinization, mucosal permeability, osmolality, cyclooxygenase-2, rat, duodenum, jejunum, motility, enteric nervous system, Fysiologi
Identifiers
urn:nbn:se:uu:diva-7444 (URN)978-91-554-6778-4 (ISBN)
Public defence
2007-02-02, B21, BMC, Norra vägen, Uppsala, 09:15
Opponent
Supervisors
Available from: 2007-01-12 Created: 2007-01-12Bibliographically approved

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